Renal Tubule Acidosis
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- Опубліковано 13 лют 2016
- This is a short video on the different types of renal tubule/tubular acidosis, or disorders in which the body cannot acidify urine.
I created this presentation with Google Slides.
Image were created or taken from Wikimedia Commons
I created this video with the UA-cam Video Editor.
ADDITIONAL TAGS:
Renal Tubule Acidosis
Acidification of the body due to inability of the kidneys to acidify urine
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Type 1: Distal
Type 4: Hyperkalemic
Type 2: Proximal
Type 1: Distal tubule RTA
Failure of the alpha-intercalated cells in distal convoluted tubule to secrete acid (H+)
Cannot acidify urine… urine pH 6ish
Decreased H+ in tubule lumen draws out K+ causing hypokalemia
Associated with Sjögren Sjogren syndrome (autoAb against CAII, which generates H+ in DCT)
Calcium phosphate kidney stones
Caused by decreased citrate excretion and hypercalciuria
Salts more likely to precipitate at higher pH
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Type 2: Proximal tubule RTA
Failure of the proximal tubule to reabsorb filtered bicarbonate
Initial insult: Excess bicarb excretion; urine pH is 6.5
After insult: Bicarb serum levels drop, impaired absorption sufficient to can still acidify urine to 5.5
Distal nephron still functions normally
NaHCO3 loss → hypoaldosteronism → mild hypokalemia
Other associated proximal tubule defects, including glucose, uric acid, phosphate, and AAs in urine (Fanconi syndrome)
Bone demineralization due to phosphate excretion; Type 2 RTA can be caused by multiple myeloma
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Type 3: Combined RTA
Patients share features of distal and proximal RTAs (types 1 and 2)
Rarely discussed
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Type 4: Hyperkalemia RTA
Caused by decreased aldosterone release or activity (hypoaldosteronism)
Decreased ENaC activity in distal tubule
Tubular lumen is less negative
Decreased excretion of K+ and H+
Hyperkalemia and acidosis
Acidosis in principal cells of DCT prevents ammoniagenesis, and NH3 is main carrier of thus urine pH is 5.5
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Summary
Type 1
Distal
Type 2
Proximal
Type 3
Combined
Type 4
Hyperkalemic
Type 1
Type 2
Type 3
Type 4
Affected physiology:
Distal convoluted tubule
Proximal convoluted tubule
PCT and DCT
Aldosterone effects on DCT
serum pH:
acidosis
acidosis
acidosis
acidosis
serum pH:
hypokalemia
hypokalemia
hypokalemia
hyperkalemia
urine pH:
6
initially 6, then 5.5
-
5.5
Associated:
High urine Ca2+, stones
Bone disorders, multiple myeloma
-
Hypoaldosteronism
Shouldn't NaHCO3 loss cause hyperaldosteronism instead of hypoaldosteronism to result in hypokalemia in type II RTA?
yes i have the same question
Yes because sodium lowers extracellular fluid volume and that initiates aldosterone secretion (hyperaldosteronis) which then leads to sodium reabsorption of Na and the K+ gets out so we have hypokalemia.
Watching this just before an exam. Thanks a lot. God bless
Best video on RTA
This was so dam good! Explained first aid where it makes sense now! Please continue to make videos.
Thank you it was a very concise and informative. Exactly what I wanted to know.
There is inc hco3- loss . Which causes decrease activity of basolateral na+ and cl- activity. Causing decreased sodium and hence hyperaldosteronism . So eventually there is hypokalemia my friend. Aldosterone causes Inc na reabsorption and potassium and H+ secretion .
Potassium and ammonia are inversely related so high potassium due to hypoaldosteron nwill cause low ammoniogenesis.
awesome, thank you
Besttttt
Thnx
I think the correct words at 1st column x 3rd line of the chart are Serum Potassium (K+) instead of Serum pH again, right?
I have sjogrens and in five years my gfr dropped 20 points I wonder if I have this. Nephrologist says she's not concerned at this point